Detection of periodontal bacterial DNA in serum and synovial fluid in refractory rheumatoid arthritis patients

Martínez-Martínez, Rita Elizabeth; Abud-Mendoza, Carlos; Patiño-Marín, Nuria; Rizo-Rodríguez, Juan C.; Little, James W.; Loyola-Rodríguez, Juan Pablo

doi:10.1111/j.1600-051x.2009.01496.x

Cited by 198 publications

(191 citation statements)

References 26 publications

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“…P. nigrescens is one of the species frequently found in subgingival plaque of aggressive periodontitis mostly at bleeding sites (35,36). Importantly, elevated levels of P. nigrescens DNA fragments have been found in RA serum and synovial fluid as well as in subgingival dental plaque of RA patients with periodontitis (19,20). Therefore, studying the role of periodontal pathogens other than P. gingivalis is crucial for a better understanding of the interaction between the two diseases.…”

Section: Discussionmentioning

confidence: 99%

“…The aim of the current study was to investigate the influence of periodontitis on clinical severity and specific histopathologic features of T cell-dependent experimental arthritis with particular focus on disease-relevant Th cell phenotype. Two periodontal bacteria, P. gingivalis and Prevotella nigrescens, of which the DNA has been detected in RA serum and synovial fluid (19,20), were compared. The data reveal exacerbation of autoimmune arthritis by periodontitis induced by both bacteria through induction of collagen-specific Th17 phenotype directly correlated with arthritic bone erosion, along with suppression of the joint-protective IL-4 by P. nigrescens in particular.…”

mentioning

confidence: 99%

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Periodontal Pathogens Directly Promote Autoimmune Experimental Arthritis by Inducing a TLR2- and IL-1–Driven Th17 Response

Aquino

Abdollahi‐Roodsaz

Koenders

et al. 2014

The Journal of Immunology

168

152

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Increasing epidemiologic evidence supports a link between periodontitis and rheumatoid arthritis. The actual involvement of periodontitis in the pathogenesis of rheumatoid arthritis and the underlying mechanisms remain, however, poorly understood. We investigated the influence of concomitant periodontitis on clinical and histopathologic characteristics of T cell–mediated experimental arthritis and evaluated modulation of type II collagen (CII)–reactive Th cell phenotype as a potential mechanism. Repeated oral inoculations of periodontal pathogens Porphyromonas gingivalis and Prevotella nigrescens induced periodontitis in mice, as evidenced by alveolar bone resorption. Interestingly, concurrent periodontitis induced by both bacteria significantly aggravated the severity of collagen-induced arthritis. Exacerbation of arthritis was characterized by increased arthritic bone erosion, whereas cartilage damage remained unaffected. Both P. gingivalis and P. nigrescens skewed the CII-specific T cell response in lymph nodes draining arthritic joints toward the Th17 phenotype without affecting Th1. Importantly, the levels of IL-17 induced by periodontal pathogens in CII-specific T cells directly correlated with the intensity of arthritic bone erosion, suggesting relevance in pathology. Furthermore, IL-17 production was significantly correlated with periodontal disease–induced IL-6 in lymph node cell cultures. The effects of the two bacteria diverged in that P. nigrescens, in contrast to P. gingivalis, suppressed the joint-protective type 2 cytokines, including IL-4. Further in vitro studies showed that the Th17 induction strongly depended on TLR2 expression on APCs and was highly promoted by IL-1. Our data provide evidence of the involvement of periodontitis in the pathogenesis of T cell–driven arthritis through induction of Ag-specific Th17 response.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Periodontal Pathogens Directly Promote Autoimmune Experimental Arthritis by Inducing a TLR2- and IL-1–Driven Th17 Response

Aquino

Abdollahi‐Roodsaz

Koenders

et al. 2014

The Journal of Immunology

168

152

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“…Furthermore, no evidences of A. actinomycetemcomitans or P. gingivalis dissemination to arthritic joints were observed (data not shown), in contrast to clinical studies that describe the presence of bacterial DNA in arthritic joints. 57,62 Another possibility is that the distinct kinetics of both chronic models (when PD is induced, PIA is already in development) are difficult for the observation of a putative effect over experimental RA severity.…”

Section: Experimental Periodontitis and Arthritis Interaction Ap Trommentioning

confidence: 99%

Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

Trombone¹,

Claudino²,

Colavite³

et al. 2010

Genes Immun

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Periodontitis (PD) and rheumatoid arthritis (RA) have been found to be clinically associated and to share the chronic nature of the inflammatory reaction associated with bone resorption activity. However, the mechanisms underlying such association are unknown. Therefore, we examined the basis of Actinobacillus actinomycetemcomitans-and Porphyromonas gingivalis-induced PD and pristane-induced arthritis (PIA) interaction in mice. Higher severity PD in the genetically inflammation prone acute inflammatory reactivity maximum (AIRmax) mice strain was associated with higher levels of TNF-a, IL-1b, IL-17, matrix metalloproteinase (MMP)-13, and RANKL, whereas PD/PIA co-induction resulted in even higher levels of IL-1b, IFN-g, IL-17, RANKL, and MMP-13 levels. Conversely, PD/PIA co-induction in AIRmin strain did not alter the course of both pathologies. PIA/PD co-induction resulted in altered expression of T-cell subsets transcription factors expression, with T-bet and RORg levels being upregulated, whereas GATA-3 levels were unaltered. Interestingly, PIA induction resulted in alveolar bone loss, such response being highly dependent on the presence of commensal oral bacteria. No differences were found in PIA severity parameters by PD co-induction. Our results show that the interaction between experimental PD and arthritis in mice involves a shared hyper-inflammatory genotype and functional interferences in innate and adaptive immune responses.

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“…Several lines of evidence indicate that the link between periodontitis and RA could be the periodontitis-associated bacteria P. gingivalis. DNA from P. gingivalis detected in serum and synovial fluid from patients with RA (30,31), and enhanced antibody titers against P. gingivalis have been found in RA patients (32,33). Moreover, periodontitis and RA have been suggested to involve citrullination of proteins by the peptidylarginine deiminase expressed by P. gingivalis, which then could drive autoimmunity in RA (34).…”

mentioning

confidence: 99%

Porphyromonas gingivalis Stimulates Bone Resorption by Enhancing RANKL (Receptor Activator of NF-κB Ligand) through Activation of Toll-like Receptor 2 in Osteoblasts

Kassem

Henning

Lundberg

et al. 2015

Journal of Biological Chemistry

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Background: Inflammation causes bone loss through enhanced osteoclast formation. Results: Porphyromonas gingivalis stimulates osteoclast formation through Toll-like receptor 2. Conclusion: Activation of Toll-like receptors may represent a mechanism for inflammation-induced bone loss in diseases like rheumatoid arthritis and periodontitis. Significance: A thorough understanding of the mechanisms involved in inflammation-induced bone loss will lead to improved treatment.

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Detection of periodontal bacterial DNA in serum and synovial fluid in refractory rheumatoid arthritis patients

Abstract: This study suggests that PBDNA could have a role on the RA aetiology. The possible pathway of transport of PBDNA from mouth to joints could be via the free form of DNA.

Cited by 198 publications

References 26 publications

Periodontal Pathogens Directly Promote Autoimmune Experimental Arthritis by Inducing a TLR2- and IL-1–Driven Th17 Response

Periodontal Pathogens Directly Promote Autoimmune Experimental Arthritis by Inducing a TLR2- and IL-1–Driven Th17 Response

Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

Porphyromonas gingivalis Stimulates Bone Resorption by Enhancing RANKL (Receptor Activator of NF-κB Ligand) through Activation of Toll-like Receptor 2 in Osteoblasts

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